Asthma, Rhinitis, Other Respiratory DiseasesRelationship between airway inflammation, hyperresponsiveness, and obstruction in asthma☆,☆☆
Section snippets
Subjects
Data had been entered into a database (Filemaker Pro 3.0, Filemaker Inc, Santa Clara, Calif) on 205 nonsmoking subjects with stable asthma who had undergone standardized 12-minute sputum induction, spirometry, and methacholine challenge during enrollment in outpatient asthma studies performed during the past 5 years at the Asthma Research Center at the University of California, San Francisco. The subject population comprised all individuals with asthma who participated in outpatient clinical
Patient characteristics
A total of 205 subjects for whom spirometry, methacholine challenge, and sputum data were available were identified (Table I).
Characteristic Value* Age (y): mean ± SD 33.0 ± 9.1 Sex: female 114 (56%) Ethnicity White 140 (68%) African American 25 (12%) Hispanic 18 (9%) Other 22 (11%) On inhaled corticosteroids 83 (40%) Percent of predicted FEV1 <60% 17 (8%) 61% to 80% 76 (37%) >80% 112 (55%) PC20: median (interquartile range) 0.41 (0.18, 1.05) *Presented as number (percent)
Discussion
Our multivariate models suggest that both eosinophilic inflammation and neutrophilic inflammation in sputum are independently associated with degree of chronic airway obstruction, as measured by FEV1. With regard to bronchial hyperreactivity, sputum eosinophilia shows a relationship with PC20 whereas sputum neutrophilia does not. The finding that sputum neutrophilia relates to FEV1 but not to PC20 was surprising. Although the mechanisms governing chronic airway narrowing and chronic airway
Acknowledgements
We thank Hofer Wong, Martha Birch, Theresa Ward, Lisa Musumeci, Elika Rad, and Jack Covington for coordination of patient enrollment and Jane Liu for her expertise in the cytologic analysis of induced sputum.
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Cited by (0)
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Financial support: Dr Woodruff is supported by the NIH Multidisciplinary Training Program in Lung Disease HL-07185 and Dr Fahy by RO1 HL-61662. Subjects were initially recruited during studies supported by the NHLBI ACRN U10 HL-51823, NR-03995, and SCOR/PPG P01 HL-56385 and during studies supported by Novartis, Boehringer-Ingelheim, Texas Biotechnology, and Pharmacia & Upjohn.
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Reprint requests: John V. Fahy, MD, Box 0130, University of California, San Francisco, 505 Parnassus Avenue, San Francisco, CA 94143.